First Report of Fusarium oxysporum f. sp. lycopersici Race 3 on Tomato in Tennessee.

In the summer of 2000, tomato (Lycopersicon esculentum Mill.) plants in several commercial fields in southeastern and eastern Tennessee exhibited symptoms of Fusarium wilt. All cultivars on which symptoms were observed are classified as resistant to races 1 and 2 of the causal fungus, Fusarium oxysporum Schlechtend.:Fr. f. sp. lycopersici (Sacc.) W.C. Snyder and H.N. Hansen. Race 3 has been reported from several areas (1), but not from Tennessee, a major producer of fresh market tomatoes. F. oxysporum was consistently isolated from discolored vascular tissue on potato dextrose agar (PDA). Pathogenicity and race determination tests for six isolates representing three counties were conducted by inoculating cultivars susceptible to races 1, 2, and 3 (Rutgers); resistant to race 1 (Bradley, Roma VF); resistant to races 1 and 2 (Conquest, Florida 47); or resistant to races 1, 2, and 3 (Floralina). Inoculum suspensions were obtained from 1-week-old cultures grown on PDA. Seedlings were grown in commercial potting mix for 3 weeks. The roots were rinsed and submerged for 30 s in inoculum suspensions (1 × 107 conidia per ml). Seedlings were then transplanted into potting mix in metal flats and placed in a greenhouse. Natural light conditions provided a 12-h photoperiod, and day and night temperatures averaged 29 and 17°C, respectively. Within 4 weeks after inoculation, all isolates caused symptoms of Fusarium wilt in all cultivars except Floralina, indicating that the isolates were race 3. The pathogen was reisolated from the discolored vascular tissue of diseased plants. Among the cultivars most severely affected by all six isolates was Conquest, which is resistant to F. oxysporum f. sp. radicis-lycopersici, the cause of Fusarium crown and root rot. Reference: (1) M. L. Marlatt et al. Plant Dis. 80:1336, 1996.

Yellow Vine of Watermelon and Pumpkin in Tennesse.

Yellow vine (YV) is a recently recognized decline of cucurbits expressed as plant yellowing, phloem discoloration, and death of vines as fruit approach maturity. In severely affected fields, YV incidence can range from 50 to 100% with similar yield loss. The disease has been associated with a phloem-limited, walled bacterium belonging to the gamma-3-proteobacteria (1), for which specific polymerase chain reaction (PCR) primers have been developed and used in diagnosis (2). First observed in 1988 in Oklahoma and Texas squash and pumpkin, YV was not detected in watermelon and cantaloupe until 1991. The disease has never been detected in cucumber. Efforts to date have been unsuccessful in transmitting the disease with dodder, grafting, or selected insects. Initially, the geographic range of the disease appeared to be generally confined to central and northeastern Oklahoma and north central Texas, an area known as the Cross Timbers Region. In 1997 to 1998, YV was diagnosed in commercial fields of watermelon and muskmelon from east Texas (Post Oak Savannah) and all cucurbit-growing areas of Oklahoma. In late summer 1998, symptoms similar to those of YV were observed in one watermelon (Hardeman County) and three pumpkin (Rhea and Morgan counties) fields in Tennessee where the leaves turned yellow and chlorotic and affected plants exhibited phloem discoloration. Estimated incidence of YV ranged from less than 1 to 20% of the plants in affected fields. PCR, with the YV-specific primers (2), amplified a band of the expected size (409 bp) from all watermelon and pumpkin plants exhibiting phloem discoloration. In contrast, no bands were amplified from asymptomatic (no phloem discoloration) watermelon or pumpkin. The nucleotide sequence of the DNA fragment amplified from a Tennessee watermelon and pumpkin plant was identical to that of the YV bacterium. The occurrence of YV outside of the Cross Timbers Region, and in a location as distant as Tennessee, suggests that the disease may be much more widespread than previously recognized. Diagnosis and monitoring of YV in all cucurbit-growing areas is critical for determining the geographic distribution and losses caused by this emerging disease. References: (1) F. J. Avila et al. Phytopathology 88:428, 1998. (2) U. Melcher et al. (Abstr.) Phytopathology. 89(suppl.):S95, 1999.

Genetic Basis of the Epidemiologic effects of Resistance to Meloidogyne incognita in the Tomato Cultivar Small Fry.

The genetic nature of resistance and its epidemiologic effects on two Meloidogyne incognita populations were assessed in the F hybrid tomato cv. Small Fry. The progeny of a Small Fry x Small Fry cross segregated in a 3:1 resistant:susceptible ratio, indicating the presence of a single, completely dominant resistance gene (LMiR) in Small Fry. In a subsequent experiment, infection frequency and the rate of development of primary infection on resistant Small Fry x Small Fry segregates were compared to those on susceptible segregates and the susceptible cultivar Rutgers. Suppression in both infection frequency and rate of development of primary infection was entirely attributable to gene LMiR. A single egg-mass population of M. incognita propagated for 12 generations on Small Fry showed an increased ability over the wild type population to parasitize plants containing the LMiR gene but failed to completely overcome resistance. The relationship of this phenomenon to the genetics of the Lycopersicon esculentum-M. incognita interaction is discussed.